Subarachnoid haemorrhage is bleeding into the space between the subarachnoid membrane and the pia mater.
It accounts for 5-10% of all strokes.
Incidence is 8-10 cases per 100 000 per year.
It is most frequent in those aged 55 to 60.
SAH accounts for 3% of patients presenting to ED with headache.
Classical presentation is a thunderclap occipital headache - "as if kicked in head"- with vomiting and neck stiffness.
Sentinel headache is now seen as less relevant.
Causes of SAH:
- ruptured berry aneurysm (75%)
- malformations (5%)
- idiopathic
- (post trauma)
Common sites of berry aneurysms are:
- junction of the posterior communicating artery with the internal carotid
- junction of the anterior communicating artery with the anterior cerebral artery
- the bifurcation of the middle cerebral artery
20% of berry aneurysms are multiple.
Subarachnoid haemorrhages are associated with:
- polycystic kidneys
- coarctation of the aorta
- Ehlers-Danlos syndrome
- PAN
- Marfans
Investigation is:
- CT - >90% of bleeds detected within 24 hrs; sensitivity declines rapidly after 10 days
- LP - done >12hrs after onset looking for xanthochromia. If the analysis of fluid will be delayed the sample should be protected from light to prevent degradation of bilirubin
Management:
- neurosurgical referral – coiling is now replacing clipping as the treatment of choice
- prompt angiography if surgery likely
- nimodipine
- possibly hyperventilation – cerebral vasculature reacts to arterial CO2 tension so lower CO2 would lower ICP
Outcome:
- 30 day mortality rate of 45%
- Predictors of mortality are age, decreased GCS on admission and large volume of blood on initial CT
- a third of survivors moderately to severely disabled
- most re-bleeds occur in the first 3 weeks
Complications:
- rebleeding
- hydrocephalus – 20%
- cardiac dysfunction
- hyponatraemia – 30%
- hypomagnesaemia – associated with poor outcome; consider replacement if <0.7mmol
Small print gem: ECG abnormalities are common and troponin is raised in up to 30% of cases. It is thought this is because of excessive myocardial catecholamine release, caused by the SAH.
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